Numerous laboratories over the past decade have shown that senescence in some strains of Fungi is caused by unstable regions in the mitochondrial and nuclear genomes. As there has been some question as to whether similar mechanisms could affect human aging, the LBG recently completed a study in which we sequenced 32,000 base pairs from 83 clones obtained from retinal tissue from a 71 year old individual. Of the 5 base pairs which varied from the published mitochondrial sequence, only one of these was heterotypic, or representative of a somatic mutation. As there are 45 cell division cycles (2 45) between a fertilized oocyte and a developed human being and given that the DNA polymerase responsible for replicating the mitochondrial genome has an error rate of about 1/6600bps, without DNA repair and other mechanisms of maintaining fidelity we would expect to find 216 mutational events in the 32 Kb sequenced. However, only one heterotypic mutation was found. This high degree of fidelity in the mitochondrial genome, as observed in the sequences cloned, raises a number of questions ranging from the possible role of DNA repair mechanisms, which are believed to be deficient in the mitochondria, to the effects of UV radiation in the retinal cells.